Relevant bibliographies by topics / Eisenmenger syndrome

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Eisenmenger syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Eisenmenger syndrome"

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Campos, Fernando Peixoto Ferraz de, and Luiz Alberto Benvenuti. "Eisenmenger Syndrome." Autopsy and Case Reports 7, no. 1 (2017): 5–7. http://dx.doi.org/10.4322/acr.2017.006.

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Arvanitaki, Alexandra, Michael A. Gatzoulis, Alexander R. Opotowsky, Paul Khairy, Konstantinos Dimopoulos, Gerhard-Paul Diller, George Giannakoulas, et al. "Eisenmenger Syndrome." Journal of the American College of Cardiology 79, no. 12 (March 2022): 1183–98. http://dx.doi.org/10.1016/j.jacc.2022.01.022.

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Previte, Joseph, and Panchapakesan Haran. "Eisenmenger Syndrome." Seminars in Cardiothoracic and Vascular Anesthesia 5, no. 1 (March 2001): 67–78. http://dx.doi.org/10.1053/scva.2001.21556.

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Beghetti, Maurice, and Nazzareno Galiè. "Eisenmenger Syndrome." Journal of the American College of Cardiology 53, no. 9 (March 2009): 733–40. http://dx.doi.org/10.1016/j.jacc.2008.11.025.

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Duke, Martin. "Victor Eisenmenger (1864–1932): The man behind the syndrome." Journal of Medical Biography 25, no. 1 (July 9, 2016): 52–55. http://dx.doi.org/10.1177/0967772014555301.

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Although much has been written about the cardiovascular abnormalities present in Eisenmenger’s syndrome, little has been recorded previously in the medical literature about Victor Eisenmenger, the Austrian doctor whose name is attached eponymously to this disorder. Archival material together with information provided by his descendants and relatives has been gathered to make available further details of his life, family, schooling, medical training and accomplishments. An examination of Eisenmenger’s book about his observations and experiences while serving from 1895 to 1914 as personal physician to Archduke Francis Ferdinand, the heir presumptive to the Austro-Hungarian throne, also sheds light on Eisenmenger’s personality, abilities and interests.
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Thiene, Gaetano. "Eisenmenger Syndrome Revisited." World Journal for Pediatric and Congenital Heart Surgery 8, no. 6 (November 2017): 726–34. http://dx.doi.org/10.1177/2150135117727259.

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Marwali, Eva M., Novik Budiwardhana, and Anna U. Rahayoe. "Inhaled prostacyclin for Eisenmenger syndrome complicated with miliary tuberculosis." Paediatrica Indonesiana 51, no. 4 (August 30, 2011): 241. http://dx.doi.org/10.14238/pi51.4.2011.241-4.

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Eisenmenger syndrome occurs in patients with large congenital cardiac or extracardiac left-to-right shunts. Clinically, Eisenmenger syndrome is characterized by multiple organ involvement and progressive deterioration of function over time. In the advanced stages, signs and symptoms of Eisenmenger syndrome include central cyanosis, dyspnea, fatigue, hemoptysis, syncope and right-sided heart failure. Survival of patients with Eisenmenger syndrome is generally poor, but appears to be better than that of patients with idiopathic pulmonary arterial hypertension (PAH) in a comparable functional class.1
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Nashat, Heba, Aleksander Kempny, Colm McCabe, Laura C. Price, Carl Harries, Rafael Alonso-Gonzalez, Michael A. Gatzoulis, Stephen J. Wort, and Konstantinos Dimopoulos. "Eisenmenger syndrome: current perspectives." Research Reports in Clinical Cardiology Volume 8 (February 2017): 1–12. http://dx.doi.org/10.2147/rrcc.s117838.

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Jeyamalar, R., V. Sivanesaratnam, and P. Kuppuvelumani. "Eisenmenger Syndrome in Pregnancy." Australian and New Zealand Journal of Obstetrics and Gynaecology 32, no. 3 (February 13, 2008): 275–77. http://dx.doi.org/10.1111/j.1479-828x.1992.tb01965.x.

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Rosenzweig, Erika B., Darryl Abrams, Mauer Biscotti, Diane Kerstein, Daphnie Drassinower, Daniel Brodie, and Matthew Bacchetta. "Eisenmenger Syndrome and Pregnancy." ASAIO Journal 64, no. 1 (2018): e8-e10. http://dx.doi.org/10.1097/mat.0000000000000548.

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Dissertations / Theses on the topic "Eisenmenger syndrome"

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Bowater, Sarah Elizabeth. "Physiological adaptations to chronic hypoxemia in Eisenmenger syndrome." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4567/.

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Eisenmenger syndrome is characterised by severe, lifelong hypoxaemia and pulmonary hypertension. Despite this, patients do surprisingly well and report a reasonable quality of life. This thesis describes a series of experiments investigating the adaptations that occur in these patients in response to the chronic hypoxaemia. Patients with Eisenmenger syndrome have severely limited exercise tolerance when assessed using cardiopulmonary exercise testing. However, they appear to maintain aerobic metabolism until late on in exercise. Studies using skeletal muscle 31P MRS during and throughout recovery from exercise showed that these patients have similar mitochondrial oxidative capacity compared to healthy controls. Echocardiography showed that patients with Eisenmenger syndrome have preserved right and left ventricular systolic function. However they have evidence of right ventricular diastolic dysfunction as evidenced by impaired early diastolic relaxation. The cardiac 31P MRS study demonstrated that despite the normal systolic function shown on echocardiography, there is impairment of septal energetics as revealed by a reduction in PCr/ATP ratio. The results presented in this thesis indicate that adult patients with Eisenmenger syndrome have undergone beneficial adaptations to the severe hypoxaemia that they are exposed to from infancy.
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Arnott, Clare. "Studies of the right ventricle and pulmonary vasculature in humans - imaging and outcomes." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17780.

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The right ventricle (RV) is the major determinant of functional capacity and prognosis in those with pulmonary arterial hypertension (PAH). Non-invasive resting and dynamic assessment of the RV, however, is inherently difficult, both at rest and during exercise. In this thesis I aimed to investigate three main issues pertaining to the RV and pulmonary vasculature in humans. Firstly, to assess the accuracy and utility of non-invasive imaging techniques in assessing the RV in health and in disease. Secondly, to define some clinically useful determinants of RV function and prognosis. Finally, I sought to report on clinical outcomes in those with increased RV afterload in the current therapeutic era, with a specific focus on differences between idiopathic PAH (IPAH) and severe PAH associated with congenital heart disease (Eisenmenger syndrome, ES) In Chapter 3 I used echocardiographic data from the Young Finns Study to assess whether intra-uterine environments and fetal development effect long term RV and LV performance. I determined that whilst those born small for gestational age (SGA) had more spherical hearts in childhood, that this difference largely attenuated in early adulthood. Whilst SGA adults had subtly dilated LV and RV parameters as compared to their normal birthweight contemporaries, these small differences were unlikely to explain the known elevated cardiovascular risk seen in the SGA group. In Chapters 4 and 5 I defined a robust, reproducible and clinically applicable exercise cardiac MRI (CMR) protocol. I employed this protocol during submaximal exercise in health and in PAH in order to report on right and left ventricular contractile reserve. I demonstrated that those with PAH have a markedly attenuated RV contractile reserve during exercise as compared to healthy subjects (PAH ΔRVEF 6% versus Controls 14%, p=0.001). Following on from this finding, I administered oxygen, a potent pulmonary vasodilator, to both groups during exercise CMR with the hypothesis that by reducing RV afterload I could improve contractile reserve in those with PAH. Importantly, neither LV or RV contractile reserve improved with the addition of oxygen therapy (p=0.60 and p=0.50 respectively). In Chapter 6, I then sought to define interventricular septal curvature (IVSC) during exertion as a more sensitive indicator of elevated RV afterload than previously used resting values. Whilst no statistically significant difference in IVSC curvature ratio (ratio of IVSC and lateral LV wall) was seen between controls and PAH patients at rest, on exertion those with PAH had markedly flatter end-systolic IVSC and abnormal curvature ratios (p=0.029). Furthermore, curvature ratio positively correlated with estimated systolic PAP (SPAP) on TTE (Spearman 1.0, p<0.001), SPAP on right heart catheter ‘RHC’ (Spearman 0.98, p=0.005), MPAP on RHC (Spearman 1.0, p<0.001), PVR on RHC (Spearman 0.9, p=0.04), and had an inverse correlation with RV contractile reserve (Spearman -0.76, p=0.046), demonstrating that those with the least contractile reserve exhibited the most abnormal curvature ratio. This was the first study to examine exertional IVSC and correlate it with clinically important imaging and invasive parameters. In the following Chapters I focus on determinants of prognosis in PAH and clinical outcomes. Firstly, in Chapter 7, I compared survival outcomes and cause of death in severe IPAH (systolic pulmonary artery pressure>80mmHg) as compared to ES. In the current era of readily available AT I found no difference in all-cause survival between the 2 groups (log rank p=0.52). An important point of difference, however, was cause of death. In the IPAH group, 75% of deaths were directly attributable to their pulmonary hypertension, as compared to only 31% in the ES group (p=0.049), who were more likely to die of complications related to their chronic cyanosis. Additionally, in Chapter 8, I analysed the presence, natural history and clinical significance of pericardial effusion (PE) in those with ES. Whilst evidence clearly states that in IPAH PE is associated with a worse prognosis, current evidence regarding its importance in ES is conflicting. I was able to determine, in 55 individuals with ES, that whilst PE was relatively common (16%), they were often small and of no haemodynamic significance, and were not associated with mortality (log rank p=0.83). Finally, in Chapter 9, I carried on from the work in Chapter 8 on determinants of prognosis in ES but was able to report on a far larger cohort (n=253) through collaboration with 12 adult congenital heart disease centres across Australia and New Zealand. We reported an 88% 5 year survival in this cohort, with a median follow-up time of 9.1 years. Importantly, we were able to demonstrate that advanced pulmonary vasodilator therapy (AT) was associated with improved survival in this group (survival HR 2.27, 95%CI 1.49-3.45; p<0.001). Taken together, the above studies contribute to the understanding of the utility and practicality of non-invasive dynamic testing in PAH, and in an understanding of clinical outcomes and factors associated with prognosis in PAH patients.
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Brabet, Monique. "Conduite à tenir anesthésique pour l'accouchement d'une patiente souffrant d'un syndrome de Eisenmenger : à propos d'un cas." Montpellier 1, 1989. http://www.theses.fr/1989MON11262.

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Clavé, Mariana Meira. "Tratamento específico em hipertensão arterial pulmonar avançada associada a cardiopatias congênitas: aspectos clínicos, bioquímicos e prognósticos." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-02072018-153122/.

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INTRODUÇÃO: A hipertensão arterial pulmonar associada a cardiopatias congênitas (HAP-CCg) é um tipo específico de doença vascular pulmonar com várias complicações. Os pacientes com HAP-CCg avançada são considerados inoperáveis e podem apresentar hipoxemia crônica e eritrocitose secundária devido ao desvio de sangue da direita para a esquerda através das comunicações cardíacas. O presente estudo teve como objetivo analisar a resposta a dois inibidores de fosfodiesterase 5 (iPDE 5), a saber, sildenafila e tadalafila, administrados por seis meses. Os fármacos haviam sido previamente aprovados para uso na HAP em geral. No entanto, a literatura é escassa no que diz respeito à sua utilização especificamente na HAP-CCg. Propusemo-nos a investigar potenciais efeitos destes fármacos além de suas ações como vasodilatadores. MÉTODOS: Foram incluídos 31 pacientes com HAP-CCg avançada (idade entre 10 e 54 anos). A maioria apresentava redução na saturação sistêmica de oxigênio, com hematócrito elevado. A sildenafila e a tadalafila foram administradas por via oral (respectivamente, 20 mg três vezes ao dia e dose única diária de 40 mg). A capacidade física foi avaliada pela distância percorrida em 6 minutos (teste de caminhada de 6 minutos, protocolo American Thoracic Society). A qualidade de vida relacionada à saúde foi avaliada utilizando-se o questionário genérico SF-36. Níveis circulantes de marcadores de disfunção microvascular foram analisados por ensaios imunoenzimáticos. Todas as medidas foram realizadas na condição basal, e aos três e seis meses de tratamento com iPDE 5. Utilizando casuística ampliada com análise de dados tanto de forma retrospectiva como prospectiva, investigamos variáveis com possível valor prognóstico. RESULTADOS: Os tratamentos com ambos os fármacos foram associados à melhora da capacidade física (classe funcional e distância percorrida em 6 minutos, p < 0,05), hematócrito e nível de hemoglobina (p < 0,05), e qualidade de vida relacionada à saúde (componentes físico e mental, p < 0,05). Comparados ao grupo controle, na condição basal, os pacientes apresentaram níveis plasmáticos elevados de beta-tromboglobulina (beta-TG, p=0,002), selectina P (p=0,018), ativador do plasminogênio tipo tecidual (t-PA, p=0,005) e do antígeno do fator de von Willebrand (VWF:Ag, p=0,005); a trombomodulina mostrou-se significantemente reduzida (TM, p < 0,001). A administração de tadalafila foi seguida de melhora no nível de beta-TG (p=0,004), t-PA (p=0,003) e TM (p=0,046), enquanto a selectina P modificou-se apenas com a sildenafila (p=0,034). O VWF:Ag mostrou-se com melhora significante, porém transitória, no grupo tratado com sildenafila (p=0,019). Usando casuística ampliada que incluiu pacientes de estudos anteriores de nosso grupo (coorte estendida de 75 indivíduos), analisamos dados coletados no início do seguimento para todos eles, assim como outros relacionados ao tratamento. Uma série de variáveis clínicas e laboratoriais foram testadas quanto à sua possível correlação com a sobrevida livre de evento (seguimento de nove anos). Nesta parte do estudo, os pacientes receberam não apenas iPDE 5 como tratamento para HAP. Alguns deles receberam antagonistas dos receptores de endotelina isoladamente, enquanto outros receberam estes medicamentos (bosentana, ambrisentana) em combinação com iPDE 5. Após realização de análises univariada, bivariada e multivariada foi possível a identificação de quatro preditores de prognóstico desfavorável: 1, menor tempo de exposição a fármacos específicos para HAP (p < 0,001); 2, classe funcional avançada na admissão (p=0,010); 3, função sistólica ventricular direita deprimida (p=0,010); e 4, níveis circulantes elevados de VWF:Ag (p=0,013). Menor tempo de exposição aos medicamentos específicos para HAP foi caracterizado como preditor independente de desfechos. CONCLUSÕES E COMENTÁRIOS: Com base nestas observações, concluímos que os iPDE 5 são importantes no manejo da HAP-CCg avançada. Os efeitos foram observados não apenas na capacidade física e na qualidade de vida, mas também em marcadores biológicos de disfunção microvascular, potencialmente relacionados à progressão e/ou complicações da doença. Além disso, as observações em longo prazo sugeriram que maior tempo de exposição aos fármacos para HAP (incluindo iPDE 5) foi benéfico, enfatizando a necessidade de instituição precoce das terapias. O fato de o estudo ter sido realizado apenas com fármacos de administração oral torna os resultados relevantes no que diz respeito a regiões onde o acesso a tratamentos específicos para HAP é limitado a tais modalidades
INTRODUCTION: Pulmonary arterial hypertension associated with congenital heart disease (CHD-PAH) is a particular form of pulmonary vascular disease with a number of complications. Patients with advanced CHD-PAH are deemed inoperable, and may present with chronic hypoxemia and secondary erythrocytosis due to right-to-left shunting across the cardiac communications. The present study was aimed at analyzing the response to 2 phosphodiesterase type 5 inhibitors (PDE5is), namely sildenafil and tadalafil, which were administered for 6 months. The drugs had been previously approved for management of PAH in general. However, there has been scarce literature on their use in the specific setting of CHD-PAH. We wished to investigate potential effects beyond their actions as vasodilators. METHODS: Thirty-one patients with advanced CHD-PAH were enrolled (age 10 to 54 years). Most of them had systemic oxygen desaturation with elevated hematocrit. Sildenafil and tadalafil were administered orally (respectively, 20 mg t.i.d and single daily dose of 40 mg). The physical capacity was assessed by registering the 6-minute walked distance (6-minute walk test, American Thoracic Society protocol). Health-related quality of life was assessed using the SF-36 generic questionnaire. Circulating levels of microvascular dysfunction markers were analyzed by enzyme-linked immunoassays. All measurements were performed at baseline, 3 months and 6 months of PDE5i administration. Using a larger patient population with retrospective as well as prospective data analysis, we looked for potential predictors of prognosis. RESULTS: Both therapies were associated with improvement of the physical capacity (functional class and 6-minute walked distance, p < 0.05), hematocrit and hemoglobin level (p < 0.05), and health-related quality of life (physical and mental components, p < 0.05). Compared to controls, patients had elevated baseline plasma levels of beta-thromboglobulin (beta-TG, p=0.002), P-selectin (p=0.018), tissue-type plasminogen activator (t-PA, p=0.005) and von Willebrand factor antigen (VWF:Ag, p=0.005), while thrombomodulin was importantly reduced (TM, p < 0.001). Tadalafil administration was followed by improvement of beta-TG (p=0.004), t-PA (p=0.003) and TM level (p=0.046), while P-selectin was improved by sildenafil only (p=0.034). VWF:Ag improved significantly, but only transiently in the sildenafil group (p=0.019). Using an extended population which included additional patients from previous studies of ours (the extended cohort consisted of 75 individuals), we analyzed data collected at the beginning of follow-up for all subjects, and treatment-related data as well. A number of clinical and laboratory parameters were tested for their possible correlation with event-free survival (9-year survival analysis). In this part of the study, patients were on monotherapy or combination therapy with PDE5is (sildenafil or tadalafil) and endothelin receptor antagonists (bosentan or ambrisentan). Univariate, bivariate and multivariate analyses were used to identify four predictors of a more worrisome prognosis: 1, a shorter time of exposure to specific PAH therapies (p < 0.001); 2, an advanced functional class at entry (p=0.010); 3, a depressed right ventricular systolic function (p=0.010); and 4, high circulating levels of VWF:Ag (p=0.013). A shorter exposure to PAH therapies was characterized as an independent predictor of poor outcome. CONCLUSIONS AND COMMENTS: Our observations point towards beneficial effects of PDE5is in advanced CHD-PAH. Importantly, the observed effects were not only on the physical capacity, and quality of life, but also biological markers of microvascular injury potentially related to disease progression and/or complications. Furthermore, long-term patient observation showed that a longer exposure to PAH drugs (including PDE5is) was beneficial, thus emphasizing the need for early initiation of therapies. Because only oral drugs were used, results may be relevant for countries and regions with limited access to PAH-specific medications
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Hascoët, Sébastien. "Thérapies avancée de l'hypertension artérielle pulmonaire associée aux cardiopathies congénitales Pumpless Lung Assist as a Bridge to Medical Therapy in a Teenager With Pulmonary Arterial Hypertension and Partial Anomalous Pulmonary Venous Return Transplantation for Pulmonary Arterial Hypertension with Congenital Heart Disease: Impact of Current Therapeutic Approach Including a High-Priority Allocation Programme on Outcomes Outcome of adults with Eisenmenger syndrome treated with drugs specific to pulmonary arterial hypertension: A French multicentre study Long-term outcomesofpulmonaryarterial hypertension underspecific drugtherapyin Eisenmenger syndrome." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASQ010.

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Résumé : Les cardiopathies congénitales sont les anomalies congénitales les plus fréquentes. Grâce aux progrès dans la prise en charge chirurgicale, environ 90% des enfants ayant une cardiopathie congénitale vivent désormais jusqu’à l’âge adulte. Néanmoins, l’évolution clinique de ces patients peut être marquée par des complications, dont l’hypertension artérielle pulmonaire. Celle-ci peut se développer secondairement à l’absence ou au retard de prise en charge dans l’enfance ou à des lésions résiduelles. L’hypertension artérielle pulmonaire est associée à un pronostic altéré, essentiellement par défaillance ventriculaire. L’hypertension artérielle pulmonaire chez ces patients se caractérise par la variabilité des aspects hémodynamiques selon les lésions anatomiques sous-jacentes. Sa prise en charge demeure variable, complexe et controversée. La correction de la cardiopathie congénitale sous-jacente est recommandée ou contre-indiquée selon la sévérité de l’hypertension artérielle pulmonaire. Les traitements spécifiques médicamenteux vasodilatateurs pulmonaires pourraient être bénéfiques dans les atteintes les plus évoluées. Les patients avec atteinte terminale pourraient bénéficier de la transplantation cardio-pulmonaire. L’objectif principal de cette thèse a été d’étudier l’impact hémodynamique et sur le pronostic des différentes approches thérapeutiques avancées actuellement disponibles pour la prise en charge de l’hypertension artérielle pulmonaire associée aux cardiopathies congénitales. Ont été étudiés en particulier les traitements médicamenteux spécifiques, la correction du shunt par voie percutanée, l’assistance circulatoire et la transplantation cardio-pulmonaire. Cette thèse a permis de montrer qu’une prise en charge pro-active de l’hypertension artérielle pulmonaire chez les patients ayant une cardiopathie congénitale est associée à une amélioration des paramètres hémodynamiques, des paramètres cliniques et par une amélioration du pronostic. Les résultats de cette thèse invitent à poursuivre le recours aux thérapies avancées et leur évaluation afin d’affiner les algorithmes de prise en charge clinique
Abstract: Congenital heart disease is the most common birth defect. Thanks to advances in surgical management, about 90% of children with congenital heart disease now live to adulthood. Nevertheless, the clinical course of these patients may be marked by complications, including pulmonary arterial hypertension. It may develop secondary to the absence or delay of treatment in childhood or to residual lesions. It is associated with an altered prognosis, primarily due to ventricular failure. Pulmonary arterial hypertension in these patients is characterized by variability in hemodynamic aspects depending on the underlying anatomical lesions. Its management remains variable, complex and controversial. Correction of underlying predisposing congenital heart disease is recommended or contraindicated depending on the degree of severity of pulmonary arterial hypertension. Specific pulmonary vasodilator drug therapies may be beneficial in more advanced disease. Patients with end stage disease may benefit from cardiopulmonary transplantation. The main objective of this thesis was to study the hemodynamic and prognostic impact of the different advanced therapeutic approaches currently available for the management of pulmonary arterial hypertension associated with congenital heart disease. Specific drug therapies, percutaneous shunt correction, circulatory support and cardiopulmonary transplant were studied. This thesis has shown that proactive management of pulmonary arterial hypertension in patients with congenital heart disease is associated with improved hemodynamic parameters, clinical parameters and improved prognosis. The results of this thesis call for further use and evaluation of advanced therapies to refine clinical management algorithms
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Luchner, Lisa [Verfasser]. "Langzeittherapie mit Bosentan bei Patienten mit Eisenmenger-Syndrom / Lisa Luchner." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1218077042/34.

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Scherber, Philipp Robert [Verfasser], and Hashim [Akademischer Betreuer] Abdul-Khaliq. "Analyse der myokardialen Funktion mit der neuen 2D-Strain Echokardiografie bei Patienten mit Eisenmenger-Syndrom vor und nach der Behandlung mit Bosentan / Philipp Robert Scherber. Betreuer: Hashim Abdul-Khaliq." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2011. http://d-nb.info/1051095875/34.

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Scherber, Philipp Robert Verfasser], and Hashim [Akademischer Betreuer] [Abdul-Khaliq. "Analyse der myokardialen Funktion mit der neuen 2D-Strain Echokardiografie bei Patienten mit Eisenmenger-Syndrom vor und nach der Behandlung mit Bosentan / Philipp Robert Scherber. Betreuer: Hashim Abdul-Khaliq." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:291-scidok-40361.

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Books on the topic "Eisenmenger syndrome"

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Thorne, Sara, and Sarah Bowater. Eisenmenger syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759959.003.0010.

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This chapter describes Eisenmenger syndrome, which can occur when there is a large, nonrestrictive communication between the systemic and pulmonary circulations. This shunt can be at atrial, ventricular, or arterial levels. The chapter discusses the natural history of Eisenmenger syndrome as well as complications, extracardiac manifestations, physical signs, investigations, and management.
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Katritsis, Demosthenes G., Bernard J. Gersh, and A. John Camm. Eisenmenger syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199685288.003.0241.

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Thorne, Sara, and Paul Clift, eds. The Eisenmenger syndrome. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199228188.003.0016.

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Introduction 114Natural history 114Complications and extra-cardiac manifestations 114Physical signs 114Investigations 116Management 116Large communication between the systemic and pulmonary circulations at atrial, ventricular, or arterial level: → high pulmonary blood flow (L-to-R shunt);→ development of high pulmonary vascular resistance;...
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Serfass, Evan R., and Justin D. Ramos. Ventricular Septal Defect. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0007.

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Ventricular septal defect (VSD) is the most common congenital cardiac lesion, and VSDs are found as isolated lesions in up to 20% of children with congenital heart disease. The natural history and pathophysiology of VSD varies by patient age, patient size, anatomic location, and size of the defect. Patients who have large lesions and significant left-to-right shunt resulting in heart failure symptoms, failure to thrive, pulmonary hypertension, or recurrent respiratory infections may be indicated for early surgical repair during infancy. This chapter presents a clinical scenario of a symptomatic infant undergoing primary surgical repair of a VSD to demonstrate principles of the anatomy, pathophysiology, diagnosis, and medical management of patients with VSDs. Anesthetic management is also discussed, considering the effects of left-to-right shunt, pulmonary hypertension, delayed sternal closure, and Eisenmenger’s syndrome.
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Dob, Daryl P., Elspeth E. Pickering, and Michael A. Gatzoulis. Moderate to complex congenital heart disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0040.

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Children born with congenital heart disease no longer face the prospect of early death and a poor quality of life. In fact, most neonates with moderate to complex congenital heart disease have a survival rate to adulthood of over 80%. The ratio of adults to children with congenital heart disease is increasing, due to better surgical repairs, and longer survival with a better quality of life. In the Western world, there are more adults than children alive with congenital heart disease. This remarkable medical effort has allowed young women with congenital heart disease to mature to an age where they wish to have babies of their own. Early generations of women, palliated with Mustard or Senning repairs, have shown it is possible to face the cardiovascular challenges of pregnancy and survive. As the number of women with congenital heart disease is predicted to grow by 25% in the next decade and more women with congenital heart disease become pregnant; a better understanding of moderate to complex heart disease, different surgical repair procedures, and residual anomalies is paramount. This chapter examines the management of parturients with transposition complexes (both classical and congenitally corrected), tetralogy of Fallot, the Fontan circulation, Eisenmenger’s syndrome, and congenital aortic stenosis, taking into consideration the effect of pregnancy, labour, delivery, and anaesthesia on each circulation.
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Book chapters on the topic "Eisenmenger syndrome"

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Gupta, Ruchi, Shirah Shore, Maria M. Rodriguez, and Marco Ricci. "Eisenmenger Syndrome." In Principles of Pulmonary Protection in Heart Surgery, 171–77. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-308-4_19.

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Michelow, Marilyn Diane. "Eisenmenger Syndrome." In Anesthesiology, 41–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50141-3_7.

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Inai, Kei, Alexander K. C. Leung, Jouni Uitto, Gerhard-Paul Diller, Michael A. Gatzoulis, John-John B. Schnog, Victor E. A. Gerdes, et al. "Eisenmenger Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 567–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_539.

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Yung, Delphine. "Pulmonary Hypertension/Eisenmenger Syndrome." In Textbook of Clinical Pediatrics, 2413–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_257.

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D’Alto, Michele, and Giovanni Maria Di Marco. "Eisenmenger Syndrome in Patients with Down Syndrome." In Pulmonary Hypertension in Adult Congenital Heart Disease, 279–89. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46028-4_18.

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Owusu-Ansah, Kevin, Zeksen Lim, and Gruschen R. Veldtman. "Pulmonary Arterial Hypertension in Eisenmenger Syndrome." In Adult Congenital Heart Disease, 57–75. Oxford, UK: Blackwell Publishing Ltd., 2009. http://dx.doi.org/10.1002/9781444311846.ch5.

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Broberg, Craig S. "Eisenmenger Syndrome: Pathophysiology and Haematologic Effects." In Pulmonary Hypertension in Adult Congenital Heart Disease, 29–44. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-46028-4_3.

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Mahli, Ahmet, and Demet Coskun. "Anesthesia for Pregnant Patients with Eisenmenger Syndrome." In Obstetric Anesthesia for Co-morbid Conditions, 219–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93163-0_15.

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Edwards, Christopher. "Pregnancy Plus Atrial Septal Defect vs Eisenmenger Syndrome." In Clinical Anesthesiology, 325–28. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8696-1_39.

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Sadeghpour, Anita, and Azin Alizadehasl. "Pulmonary Hypertension Associated with Congenital Heart Disease, Eisenmenger Syndrome." In Comprehensive Approach to Adult Congenital Heart Disease, 117–24. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6383-1_15.

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Conference papers on the topic "Eisenmenger syndrome"

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Anderson, D. K., and C. E. Bennett. "Recurrent Hemoptysis in the Setting of Eisenmenger Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6754.

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Tacer, Ana, Nejc Pavsic, Polona Koritnik, Katja Prokselj, TT Schlegel, and Vito Starc. "High-Resolution Electrocardiography in Patients with Eisenmenger Syndrome." In 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662871.

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Rowan, CA, D. Lederer, KS Lee, and EB Rosenzweig. "Ambrisentan: Safety and Efficacy in the Treatment of Eisenmenger Syndrome." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4919.

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Dai, Z. K., I. C. Chen, J. H. Hsu, Y. H. Wu, and Y. C. Liu. "The Long Term Experience on Treatment for Adult Patients with Eisenmenger Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5075.

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Papalexiou, P., G. Karpetas, M. Spyraki, E. Dimitriou, S. Antoniou, A. Zotou, and A. Siampalioti. "B252 Combination of peripheral nerve blocks in a patient with eisenmenger syndrome." In ESRA Abstracts, 39th Annual ESRA Congress, 22–25 June 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/rapm-2022-esra.326.

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Barst, Robyn J., D. Dunbar Ivy, Erika Rosenzweig, Aimee J. Foreman, Michelle Turner, Leslie A. Meltzer, and Michael McGoon. "Characteristics And Four-Year Outcomes Of Patients With Eisenmenger Syndrome In REVEAL." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4793.

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Zebadua, R., J. C. López, N. G. Zayas, J. Sandoval, M. Villalobos-Pedroza, A. Cruz, D. K. Hernández, J. F. Canul, T. Pulido, and N. G. Zayas Hdz. "Long-term clinical assessment in patients with Eisenmenger Syndrome treated with macitentan." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.4261.

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Yang-Ting, S., J. Aboulhosn, JS Child, XG Sun, and KE Sietsema. "Effect of Pulmonary Vasodilator Therapy on Ventilatory Efficiency in Adults with Eisenmenger Syndrome." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2044.

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Chao, A., P. Chan, D. Shavelle, S. Ganesh, and B. Yaghmour. "Embolic Acute Myocardial Infarction in Young Adult with Congenital Heart Disease and Eisenmenger Syndrome." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1925.

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Sathianandan, Sobitha, Bhavin Rawal, Heba Nashat, Laura Price, Simon Padley, Kostas Dimopoulos, Tom Semple, and John Wort. "A retrospective review of computed tomography (CT) findings in Eisenmenger Syndrome and their prognostic implications." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4757.

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You might also be interested in the extended bibliographies on the topic 'Eisenmenger syndrome' for particular source types:
Journal articles
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